Shakibamaram Ghazaleh, Dolikhani Mohammadreza, Moussavi Farideh, Sarraf Syna, Benyamin Bredsin, Advani Soroor
Medical School of Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Pediatric Department, Shohada-e Tajrish Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Cancer Rep (Hoboken). 2025 Jun;8(6):e70235. doi: 10.1002/cnr2.70235.
Wernicke encephalopathy (WE) is a life-threatening neurological disorder caused by thiamine deficiency, commonly associated with alcoholism but also observed in malnourished pediatric cancer patients undergoing intensive chemotherapy. WE remains underdiagnosed in children, with many cases only confirmed postmortem. We report a 6-year-old girl with acute lymphoblastic leukemia (ALL) who developed WE secondary to treatment-resistant nausea and vomiting.
The patient presented with acute gait disturbance, ophthalmoparesis, and paraparesis following persistent vomiting and significant weight loss. Initial diagnostic evaluations, including cerebrospinal fluid analysis and neuroimaging, suggested alternative diagnoses such as cerebellitis and Guillain-Barré Syndrome. However, progressive neurological deterioration, the emergence of encephalopathy, and follow-up magnetic resonance imaging (MRI) findings of hyperintense lesions in the periventricular, periaqueductal, and cerebellar regions supported the diagnosis of WE. The overlapping features with other neurological conditions contributed to a delay in recognizing WE and initiating thiamine therapy. Despite initiating high-dose intravenous thiamine, symptom resolution was significant but partial. Unfortunately, the patient later developed lymphomatous meningitis and sepsis and ultimately succumbed to complications.
This case highlights the importance of early clinical recognition of WE in pediatric leukemia patients with prolonged vomiting, as delayed diagnosis can lead to irreversible neurological damage or death. Given the limitations of early neuroimaging findings, clinical suspicion should prompt immediate thiamine supplementation. The report points out the need for heightened awareness of thiamine deficiency in pediatric oncology, emphasizing the role of prophylactic supplementation in high-risk patients.
韦尼克脑病(WE)是一种由硫胺素缺乏引起的危及生命的神经系统疾病,通常与酒精中毒有关,但在接受强化化疗的营养不良的儿科癌症患者中也有观察到。儿童韦尼克脑病仍未得到充分诊断,许多病例仅在尸检后才得到证实。我们报告一名6岁急性淋巴细胞白血病(ALL)女孩,因治疗抵抗性恶心和呕吐继发韦尼克脑病。
该患者在持续呕吐和显著体重减轻后出现急性步态障碍、眼球运动麻痹和双侧下肢轻瘫。包括脑脊液分析和神经影像学检查在内的初步诊断评估提示为其他诊断,如小脑炎和吉兰-巴雷综合征。然而,进行性神经功能恶化、脑病的出现以及后续磁共振成像(MRI)显示脑室周围、导水管周围和小脑区域的高强度病变支持韦尼克脑病的诊断。与其他神经系统疾病的重叠特征导致韦尼克脑病的识别和硫胺素治疗的启动延迟。尽管开始使用高剂量静脉注射硫胺素,症状有显著但部分缓解。不幸的是,患者后来发展为淋巴瘤性脑膜炎和败血症,最终死于并发症。
本病例强调了在长期呕吐的儿科白血病患者中早期临床识别韦尼克脑病的重要性,因为延迟诊断可能导致不可逆转的神经损伤或死亡。鉴于早期神经影像学检查结果的局限性,临床怀疑应促使立即补充硫胺素。该报告指出需要提高对儿科肿瘤学中硫胺素缺乏的认识,强调预防性补充在高危患者中的作用。